Mechanisms of resistance of human small cell lung cancer lines selected in VP-16 and cisplatin

Cancer. 1996 May 1;77(9):1797-808. doi: 10.1002/(SICI)1097-0142(19960501)77:9<1797::AID-CNCR7>3.0.CO;2-9.

Abstract

Background: The combination of VP-16 and cisplatin is one of the most active regimens available for the treatment of small cell lung cancer (SCLC), however, most tumors eventually become resistant to these drugs.

Methods: To investigate the problem of resistance to VP-16 and cisplatin in patients with SCLC, we established two resistant sublines from the drug sensitive human SCLC line, NCI-H209, by in vitro selection in VP-16 and cisplatin.

Results: The VP-16-selected cell line, H209/VP, was more than 100-fold resistant to VP-16, and displayed cross-resistance to VM-26 and other topoisomerase II interactive drugs, but not to vinca alkaloids. There was no difference in accumulation of VP-16 in H209/VP compared with its parent cell line. The level of topoisomerase II-alpha was reduced to 8% of that in the parent cell line, and there was an altered form of this enzyme with a molecular weight of 160 kilodaltons (kDa), in addition to the normal 170 kDa protein. The cisplatin-selected cell line, H209/CP, was 11.5-fold resistant to cisplatin, with only a low level of cross-resistance to other platinum compounds including carboplatin, tetraplatin, iproplatin, and lobaplatin. This line was highly cross-resistant to vinca alkaloids, but not to anthracyclines or epipodophyllotoxins. The H209/CP cell line was not resistant to cadium chloride, suggesting that alterations in metallothionein are unlikely to be a cause of resistance. Although glutathione (GSH) levels were increased nearly 2-fold in H209/CP, there was no difference in levels of the GSH-related enzymes glutathione-S-transferase, glutathione peroxidase, and glutathione reductase, compared with the parent line. The H209/CP line had a 1.4-fold elevation of topoisomerase II-alpha. The accumulation of cisplatin was reduced in this cell line, and there were fewer DNA-interstrand cross links formed in the presence of cisplatin in H209/CP, compared with the parent line. Neither H209/VP nor H209/CP expressed MDR1, the gene for P-glycoprotein. The MRP gene was expressed at a slightly higher level in the H209/VP cell line, but there was no significant increase in expression of this gene in the H209/CP cell line.

Conclusions: The resistance of the H209/VP cell line is associated with an alteration of topoisomerase II-alpha, whereas the resistance in the H209/CP line is associated with reduced drug accumulation.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B, Member 1 / genetics
  • Antibiotics, Antineoplastic / pharmacology
  • Antibiotics, Antineoplastic / therapeutic use
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use*
  • Antineoplastic Agents, Phytogenic / pharmacology
  • Antineoplastic Agents, Phytogenic / therapeutic use*
  • Cadmium / pharmacology
  • Cadmium / therapeutic use
  • Cadmium Chloride
  • Carcinoma, Small Cell / drug therapy*
  • Carcinoma, Small Cell / enzymology
  • Carcinoma, Small Cell / physiopathology
  • Cell Line
  • Chlorides / pharmacology
  • Chlorides / therapeutic use
  • Cisplatin / pharmacology
  • Cisplatin / therapeutic use*
  • Cross Reactions
  • DNA / drug effects
  • DNA Topoisomerases, Type II / analysis
  • DNA Topoisomerases, Type II / pharmacology
  • DNA Topoisomerases, Type II / therapeutic use
  • Drug Resistance, Neoplasm / genetics
  • Drug Resistance, Neoplasm / physiology
  • Etoposide / pharmacology
  • Etoposide / therapeutic use*
  • Gene Expression Regulation, Neoplastic
  • Glutathione / analysis
  • Glutathione Peroxidase / analysis
  • Glutathione Reductase / analysis
  • Glutathione Transferase / analysis
  • Humans
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / enzymology
  • Lung Neoplasms / physiopathology
  • Metallothionein / metabolism
  • Platinum Compounds / pharmacology
  • Platinum Compounds / therapeutic use
  • Podophyllotoxin / pharmacology
  • Podophyllotoxin / therapeutic use
  • Teniposide / pharmacology
  • Teniposide / therapeutic use
  • Tumor Cells, Cultured
  • Vinca Alkaloids / pharmacology
  • Vinca Alkaloids / therapeutic use

Substances

  • ATP Binding Cassette Transporter, Subfamily B, Member 1
  • Antibiotics, Antineoplastic
  • Antineoplastic Agents
  • Antineoplastic Agents, Phytogenic
  • Chlorides
  • Platinum Compounds
  • Vinca Alkaloids
  • Cadmium
  • Etoposide
  • DNA
  • Metallothionein
  • Teniposide
  • Glutathione Peroxidase
  • Glutathione Reductase
  • Glutathione Transferase
  • DNA Topoisomerases, Type II
  • Glutathione
  • Cadmium Chloride
  • Podophyllotoxin
  • Cisplatin